It's all about a mutation of genome.
The scientists focused on one of the mutated genes and traced its evolution through its appearance in the human genome.
Results of the study suggest that selective pressure from infectious pathogens such as gonorrhea might have been the reason behind the emergence of this gene variant in homo sapiens and paved the way for grandparents' existence in humans' social structures.Interestingly, humans are the only species known to live after menopause.
And now, researchers are trying to understand the longer-term health of humankind by examining mutated genomes. The new study is significant for revealing that humans picked up an additional mutated form of CD33 that lacks the sugar-binding site somewhere along the evolutionary line. CD33 is a receptor expressed in immune cells and normally binds to sialic acid, a form of sugar that covers all human cells.
The sialic acids on damaged cells and plaques no longer cause the mutant receptor to respond, allowing the microglia to break them down. Eventually, several studies have shown that this CD33 variation is protective against late-onset Alzheimer's disease. Researchers searched for clues to discover when this gene variation originally emerged and discovered signs of strong positive selection, indicating that something was pushing the gene to develop more quickly than anticipated. Additionally, they found that our closest evolutionary ancestors, the Neanderthals, and Denisovans, did not have this specific variant of CD33 in their genomes.
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